This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Very little is known about the role of SG formation in controlling viral infection. It is known that SG form in both herpes and alphavirus infected cells. While these studies are intriguing, they did not address different viral strains, the affect of interferon on SG formation or the individual contribution of TIA-1 or TIA-R in SG formation. By using TIA-1 or TIA-R knockout cell lines we have preliminary data that TIA-R is not involved in the innate response against herpes simplex 1 (HSV1) whereas TIA-1 plays a critical role in limiting HSV1 production (i.e. viral titers for HSV1 are similar in both wild type cells and TIA-R-/- cells, but significantly higher in TIA-1-/- cells). Immune preciptations (IP) were performed to identify viral proteins that affect SG formation. To date no viral proteins have been identified.